Sunday, March 31, 2013

Abstract: Fresh fruits and vegetables can harbor large and diverse populations of bacteria. However, most of the work on produce-associated bacteria has focused on a relatively small number of pathogenic bacteria and, as a result, we know far less about the overall diversity and composition of those bacterial communities found on produce and how the structure of these communities varies across produce types. Moreover, we lack a comprehensive view of the potential effects of differing farming practices on the bacterial communities to which consumers are exposed. We addressed these knowledge gaps by assessing bacterial community structure on conventional and organic analogs of eleven store-bought produce types using a culture-independent approach, 16 S rRNA gene pyrosequencing. Our results demonstrated that the fruits and vegetables harbored diverse bacterial communities, and the communities on each produce type were significantly distinct from one another. However, certain produce types (i.e., sprouts, spinach, lettuce, tomatoes, peppers, and strawberries) tended to share more similar communities as they all had high relative abundances of taxa belonging to the family Enterobacteriaceae when compared to the other produce types (i.e., apples, peaches, grapes, and mushrooms) which were dominated by taxa belonging to the Actinobacteria, Bacteroidetes, Firmicutes, and Proteobacteria phyla. Although potentially driven by factors other than farming practice, we also observed significant differences in community composition between conventional and organic analogs within produce types. These differences were often attributable to distinctions in the relative abundances of Enterobacteriaceae taxa, which were generally less abundant in organically-grown produce. Taken together, our results suggest that humans are exposed to substantially different bacteria depending on the types of fresh produce they consume with differences between conventionally and organically farmed varieties contributing to this variation.

Tuesday, March 26, 2013

DNA sequencing continues to go crazy in terms of lower cost, higher speed, and spread of technology. Alas, some aspects of doing a genome project are not necessarily keeping up. So I am posting here to ask a simple question about one of these steps. What do people out there think about the steps of getting genome / metagenome data into Genbank. Without wanting to bias answers too much - we are having some challenges in this area.
Storify of Twitter responses below the fold

Monday, March 25, 2013

At the recent "Future of Genomic Medicine" meeting, George Church gave me some grief over my "Overselling the microbiome award" because he thinks (rightly) that some people also undersell the microbiome.

Holy crap. That sounds awesome. Except that there are all correlations so far with no known causative role at least in humans.

Then they list some of the other good things microbes apparently have been proven to do:

"ANXIETY-BUSTING GUT BACTERIA""It seems that the type of bugs you have in your body can affect mood."

Though at least in this section they do refer to a mouse study but clearly imply this is true in humans too. It may be. But I am unaware of any studies proving it.

"BUGS ARE GOOD FOR YOUR SKIN""It's a common misconception that the cleaner the skin, the better — and the bacteria that live on our skin have an important role."
I am all for not killing all microbes willy nilly but their is certainly one part of the body that you probably do want to wash a lot - your hands. So As long as they don't say "Don't wash your hands" this could be OK.

So what do they say next:

‘If you wash your hands repeatedly, they dry out — this is partly because you wash away all the oils but also because you remove a large number of the bacteria that help maintain the skin’s condition,’ says Professor Mark Fielder, a medical microbiologist at Kingston University.

Oh FFS now they are basically telling people to not wash their hands.

"SHARE A KISS... AND BACTERIA"‘Every time you kiss, for example, you exchange a million bacteria. 'So your gut microbiology becomes close to that of your loved ones.’

Sounds great. I could not find any references on the topic but sounds great.

"SOME TYPES MAY PREVENT STROKE"
Wherein the tell a story based on a press release which had led me to post the following: "Award: Ridiculous, absurd, offensive overselling of the microbiome from Chalmers & Gothenburg". Any idea if I think this is an accurate press release?

Lawrence Brandt, a professor of medicine and surgery at New York’s Albert Einstein College of Medicine, believes the treatment could work for other, non-gastro conditions, such as obesity and Parkinson’s.

Seriously? Fecal transplants for Parkinson's?

And it goes on and on including:"SOME BACTERIA KEEP YOU SLIM"
"BUGS THAT HELP MEDICINE WORK""COULD THEY WARD OFF CANCER?""KEY TO BABIES’ IMMUNITY"

I mean - I really really do think the microbiome plays roles in many many parts of our lives. But those who promote it this much are the snake oil sellers of the modern era. A slight of hand here and soon they will be selling us some specific brand of probiotic or way to protect our microbiomes. So for this article the Daily Mail is getting my first multiple "Overselling the microbiome award." They could get 3 or 4 just from this article if not more. But I will just give them two. And I will keep searching for an underselling the microbiome recipient.

Sunday, March 24, 2013

Last week David Coil in my lab reminded me that he had been wanting to borrow a copy of "The Immortal Life of Henrietta Lacks" by Rebecca Skloot. I have read the book many many times and had told David I even had a preprint that Skloot or her publicist sent me before the book came out (I did not know Skloot then - I just got it because of my blog). As I went to grab the preprint off my shelf in my office he said he wanted to read it know because the genome of the HeLa cells which had been taken from Mrs. Lacks had been published a few days before. I was shocked. I asked him if he knew if the authors of said paper had gotten consent before publishing it. So I opened a web browser and googled and found the paper and some news stories and a press release from the group who did the sequencing.

Holy fuck. They did not seem to have permission. Uggh. I had thought about this a lot because a few years ago I was thinking of writing a review of "The Immortal Life of Henrietta Lacks". As part of that started to write about the possibility of sequencing the HeLa genome and what that might mean. I also did an April Fools joke relating to the topic: http://therealhela.blogspot.com. And every time new sequencing technology comes along I have thought about - and discussed with others - the possibility of sequencing the HeLa genome. And every time I got to this point I decided that it would be unethical, inappropriate, and downright stupid to do this without consent. Note - my original plans for the book review involved a focus on the strange balance between openness and sharing in the history of HeLa and the lack of consent (e.g., see this blog post).

The sequencing of #HeLa genome w/o family consent is appalling - I literally feel like throwing up @downfortylove
— Jonathan Eisen (@phylogenomics) March 18, 2013

And after that there was remarkably little discussion of the issue by others. What the fuck? People get up in arms about all sorts of minor things so why not get up in arms about this? Where were all the supposed genomic ethicists out there? How did this happen?
Thankfully, yesterday a piece on the topic came out from Rebecca Skloot (it was in this mornings New York Times) and it has launched this issue into a much more public discussion. So much discussion that I decided to storify it. See below.

Lots of discussions going on out there. And I think Rebecca deserves credit for writing this piece and bringing the story out more. I tried to get people going on Twitter and it was a slog -- people did not seem that interested to be honest. Now - everyone seems interested. Including some who say they agree with Rebecca (and me) that it was a mistake to publish this genome.

Alas, am wondering what these people thought before the Skloot article. Why did so many people just stand by and say nothing? Too busy? Did not occur to them that this could be an issue? Or something else. Oh - and why did it not occur to Francis Collins and all the people behind encode that this could be an issue. They published a lot of genomic data from HeLa cells and never once asked for consent or apparently even thought about it.

Anyway - it's about time we as a community got off our butts and started discussion how to deal with the ethics of personal genome data. This data will be coming out more and more. We need to figure out how to handle it and the consent issues around it. And we also need to do a better job of figuring out what to do with samples for which consent was not given but which are used. Should we stop using HeLa cells? Possibly. If we want consent to use them - who will give it? I don't know the answers. But I do know one thing - science should not simply proceed forward just because these questions are hard to answer. Publishing the genome without consent or talking to the family was a very very very bad idea given that the ethical issues around consent here are murky.

UPDATE - 5 PM 3/24/13

Adding some notes about the press release and genome publication

Genome paper: - some key quotes of interest

Abstract

“To date, no genomic reference for this cell line has been released, and experiments have relied on the human reference genome”

“Our results provide the first detailed account of genomic variants in the HeLa genome, yielding insight into their impact on gene expression and cellular function as well as their origins.”

The read data are available in the European Nucleotide Archive (ENA) database under the accession number ERP001427.

We report a compendium of genomic variation (CN, SNVs and SVs) as well as the first HeLa genome draft, which are available as VCF and FASTA files respectively

We provide a tool to perform the translation of coordinates between GRch37 and our HeLa reference,

Most variants in these HeLa cells thus represent common variants in the human population. The African-American population (to which Henrietta Lacks belonged) is spread between the African and European clusters, with the HeLa sample overlapping both. This demonstrates that although the genomic landscape of HeLa is strikingly different from that of a normal human cell, the population-specific SNV patterns are still detectable.

Discussion

Since the establishment of the HeLa cell line in 1952, it has been used as a model for numerous aspects of human biology with only minimal knowledge of its genomic properties. Here we provide the first detailed characterization of the genomic landscape of one HeLa line relative to the human reference genome

“The results provide the first detailed sequence of a HeLa genome,” explain Jonathan Landry and Paul Pyl from EMBL, who carried out the research. “It demonstrates how genetically complex HeLa is compared to normal human tissue. Yet, possibly because of this complexity, no one had systematically sequenced the genome, until now.”

“The HeLa genome had never been sequenced before, and modern molecular genetic studies using HeLa cells are typically designed and analysed using the Human Genome Project reference. This, however, misrepresents the sequence chaos that characterises HeLa cells, since they were derived from a cervical tumour and have since been adapting in laboratories for decades.”

Can we infer anything about Henrietta Lacks or her descendants from this sequencing?

No, we cannot infer anything about Henrietta Lacks’ genome, or of her descendants, from the data generated in this study. Firstly, the subtype of HeLa cells sequenced in this study has spent decades in labs, dividing and thus undergoing mutations and changes – they are very different from the original cells that started growing in 1951. Secondly, these initial HeLa cells were taken from Henrietta Lacks’ cervical cancer tumour – as cancer is a disease of the genome, the DNA of cancer cells is usually different to that of the patient. Without any genetic information from the http://www.genomeweb.com/blog/learnt-lessonsoriginal tumour or from Henrietta Lacks, it is impossible to distinguish which parts of the genome sequenced here originate from Mrs. Lacks, her tumour, or laboratory adaptation. The goal of this study was not to gain insights into Henrietta Lacks’ cancer or personal biology, but rather to provide a resource for researchers using HeLa cells.

The report was release on October 2012 but got very very little coverage and I have never seen/heard it mentioned anywhere. But it covers a lot of ground of direct relevance to this HeLa story. The whole report is available here.
Here are some choice statements (bolding by me)

"Large-scale collections of genomic data raise serious concerns for the indi- viduals participating. One of the greatest of these concerns centers around privacy: whether and how personal, sensitive, or intimate knowledge and use of that knowledge about an individual can be limited or restricted (by means that include guarantees of confidentiality, anonymity, or secure data protec- tion). Because whole genome sequence data provide important insights into the medical and related life prospects of individuals as well as their relatives— who most likely did not consent to the sequencing procedure—these privacy concerns extend beyond those of the individual participating in whole genome sequencing. These concerns are compounded by the fact that whole genome sequence data gathered now may well reveal important information, entirely unanticipated and unplanned for, only after years of scientific progress."

"Whole genome sequencing dramatically raises the privacy stakes because it necessarily involves examining and sharing large amounts of biological and medical information that is not only inherently unique to a single person but also has implications for blood relatives. Genomic information is inherited and determines traits like hair and eye color. Unlike a decision to share our hair or eye color, which does not reveal anything about our relatives that is not observable, a decision to learn about our own genomic makeup might inadvertently tell us something about our relatives or tell them something about their own genomic makeup that they did not already know and perhaps do not want to know. More than other medical information, such as X-rays, our genomes reveal something both objectively more comprehensive and subjectively (to many minds) more fundamental about who we are, where we came from, and the health twists and turns that life might have in store for us."

"Because whole genome sequence information directly implicates relatives, psychological harms often are not limited to the person whose genome is voluntarily being sequenced and publicly disclosed. Even individuals who learn that they do not carry a harmful variant may experience “survivor’s guilt” if another family member is affected."

"At the same time, individuals have a responsibility to safeguard their privacy as well as that of others, by giving thoughtful consideration to how sharing their whole genome sequencing data in a public forum might expose them to unwanted incursions upon their privacy and that of their immediate relatives. To be indifferent to the implica- tions of disclosure of sensitive data and information about one’s self is to act irresponsibly. That being said, it can be good and virtuous to share sensitive data about oneself in appropriate circumstances, for example, for the good of public health research or public education."

"Risks might also fall to blood relatives of these individuals who carry similar genomic variants, thereby raising the stakes of privacy concerns in whole genome sequencing compared with most other types of research."

In summary, the point of the project was to (1) start generating some reference genomes for microbes from the built environment and (2) to engage undergraduates at UC Davis in genome sequencing and microbiology of the built environment projects.

The papers are published in a new open access journal from the American Society for Microbiology called "Genome Announcements".

Thanks also to the Alfred P. Sloan Foundation which funds microBEnet and to the UC Davis Genome Center DNA Technologies Core facility which ran the sequencing. More papers are coming. Stay tuned.

And it is very very cool. My lab has been working with / collaborating with / wanting to be like Erik Matsen for a few years now and this paper is one of the reasons why. In this paper Matsen and Evans detail some really powerful and fascinating tools for phylogeny driven analysis of microbial communities.

Edge principal component analysis (edge PCA)

"enables the detection of important differences between samples that contain closely related taxa". (from the abstract)

"applies the standard principal components construction to a “data matrix” generated from the differences between proportions of phylogenetic placements on either side of each internal edge of the reference phylogenetic tree." (from the Introduction)

Squash clustering:

"outputs a (rooted) clustering tree in which each internal node corresponds to an appropriate “average” of the original samples at the leaves below the node. Moreover, the length of an edge is a suitably defined distance between the averaged samples associated with the two incident nodes, rather than the less interpretable average of distances produced by UPGMA, the most widely used hierarchical clustering method in this context". (from the Abstract)

is hierarchical clustering with a novel way of merging clusters that incorporates information concerning how the data sit on the reference phylogenetic tree (from the Introduction)

The phylogenetic distribution of reads for a given sample determines its position in the principal components projection. For the first axis, reads that fall below edges with positive coefficients on that axis' tree (marked in orange on the tree) move the corresponding sample point to the right, while reads that land on edges with negative coefficients (marked in green on the tree) move the corresponding sample point to the left. The second axis is labeled with a subtree of the first tree (the position of which is marked with a star on the first principal component tree): reads below edges with positive coefficients move sample points up, while reads below edges with negative coefficients move sample points down. The principal components shown here are the actual principal components for the example shown in Figures 4, 5, and 6.

Figure 3. How the edge PCA algorithm works.

show more

(a) For every edge of the tree, the difference is taken between the number of reads on the non-root side the number of reads on the root side (root marked with a star). (b) The results of this are put into a matrix corresponding to the sample number (row) and the edge number (column). (c) The standard PCA algorithm is then applied, resulting in a collection of eigenvectors (the principal components) and eigenvalues. (d) These eigenvectors are indexed by the edges of the tree, and hence they can be mapped back onto the tree.

Figure 2. A visual depiction of the squash clustering algorithm.

When two clusters are merged, their mass distributions are combined according to a weighted average. The edges of the reference tree in this figure are thickened in proportion to the mass distribution (for simplicity, just a subtree of the reference tree is shown here). In this example, the lower mass distribution is an equal-proportion average of the upper two mass distributions. Similarities between mass distributions, such as the similarity seen between the two clusters for the G. vaginalis clade shown here, are what cause clusters to be merged. Such similarities between internal nodes can be visualized for the squash clustering algorithm; the software implementation produces such a visualization for every internal node of the clustering tree. Note that in this figure only the number of reads placed on each edge is shown, although each placement has an associated location on each edge when performing computation.

Anyway - check out the paper. And follow their work - this is some pretty cool stuff.

UPDATE 3/21 - switched the captions for Figure 2 and 3 as per Matsen's comment that the legends were switched in production of the paper.

From Josh Neufeld's lab this paper describes a series of tools for automation of microbial diversity analyses.

Abstract:BackgroundAlthough high-throughput sequencing of small subunit rRNA genes has revolutionized our understanding of microbial ecosystems, these technologies generate data at depths that benefit from automated analysis. Here we present AXIOME (Automation, eXtension, and Integration Of Microbial Ecology), a highly flexible and extensible management tool for popular microbial ecology analysis packages that promotes reproducibility and customization in microbial research.FindingsAXIOME streamlines and manages analysis of small subunit (SSU) rRNA marker data in QIIME and mothur. AXIOME also implements features including the PAired-eND Assembler for Illumina sequences (PANDAseq), non-negative matrix factorization (NMF), multi-response permutation procedures (MRPP), exploring and recovering phylogenetic novelty (SSUnique) and indicator species analysis. AXIOME has a companion graphical user interface (GUI) and is designed to be easily extended to facilitate customized research workflows.ConclusionsAXIOME is an actively developed, open source project written in Vala and available from GitHub (http://neufeld.github.com/axiome) and as a Debian package. Axiometic, a GUI ￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼￼companion tool is also freely available (http://neufeld.github.com/axiometic). Given that data analysis has become an important bottleneck for microbial ecology studies, the development of user-friendly computational tools remains a high priority. AXIOME represents an important step in this direction by automating multi-step bioinformatic analyses and enabling the customization of procedures to suit the diverse research needs of the microbial ecology community.

Workflows like this are what many many people need. I note - I have not used this yet but it looks promising. It has some parallels to the WATERS workflow package that came from my lab a few years ago (see more about it here: http://phylogenomics.wordpress.com/software/waters/.) Alas WATERS is no longer being actively developed. Anyway - AXIOME has additional features and certainly seems like it would be useful to many people.

Monday, March 18, 2013

I am on a committee at UC Davis that is part of an National Science Foundation "ADVANCE" grant that UC Davis' Chancellor Linda Katehi and others at UC Davis received last year. The goal of the project is "increasing the participation of women, especially Latinas, in academic science, technology, engineering and mathematics careers."

One of the things the committee I am on is charged with is looking into how the policies and practices of tenure review might differentially impact women and minorities. So - related to that I am writing to ask if people out there have examples of what one might call "family friendly" policies relating to extending the amount of time one is allowed before tenure review occurs. Some questions I would love answers to for various institutions:

What are the policy guidelines for tenure review?

Can the tenure clock be extended for family related issues (e.g., birth of a child, adoption of a child, dependent medical care, etc)?

What is the specific wording of such policies?

How are such policies explained to tenure review committees and letter writers?

For UC Davis here is what I have been able to find (well, with help from the other people on the committee)

Sunday, March 17, 2013

Not sure what the basis for this is but when I start typing in a Web address in Safari on my laptop(s), the system attempts to autocomplete the address. Useful in many cases. A bit annoying in others. So I decided to see where autocomplete takes me for each letter of the alphabet. Not sure how often this changes or that the basis for it is ...but it does say something about sites I visit often. A bit scary that so many of these are from goggle .. but they do run the world I suppose ...

Alas most of these have some issues - some more than others. Going through them one by one

Untangling Life's Origins. Link to an outside PR about work supported by NSF. Not so bad - some painful stuff in the PR like the following:

“They are not the standard trees that people see in phylogenetic analysis,” he said. “In phylogenetic analysis, usually the tips of the trees, the leaves, are organisms or microbes. In these, they are entire biological systems.”

But overall reasonably tolerable compared to the others.

Home Toxic Home. Link to an outside PR. Filled with really painful stuff. Some examples

"Most organisms would die in the volcanic sulfur pools of Yellowstone and Mount Etna. Robust simple algae call it home, and their secrets to survival could advance human medicine and bioremediation. " Everything could advance human medicine and just about any other topic if you stretch it. And it is a big stretch to find any connections here.

"Michael Garavito, Michigan State University professor of biochemistry and molecular biology was part of a research team that revealed how primitive red algae use horizontal gene transfer, in essence stealing useful genes from other organisms to evolve and thrive in harsh environments. " Ahh. Back to the same general story that got me riled up to begin with. This also has the fun "primitive" reference for algae which are not in any obvious way primitive.

"The algae’s membrane proteins are biologically quite interesting because they’re receptors and transporters, the same classes of proteins that play key roles in energy metabolism and human immune response,” said Garavito. “This has applications in human medicine because virtually all of the important pathways that contribute to disease treatment involve membrane proteins." So let me get this straight. The algae has membrane transporters and receptors. And therefore it is relevant to studies of human disease because many diseases are due to problems in transporters and receptors. So - what organism on the planet then would not be relevant? Uggh.

They then clarify "What makes the algae’s membrane proteins attractive as a model for humans is their robustness. Other traditional candidates, such as yeast, insect cell cultures and slime mold, are fragile. The algae give researchers extra time to manipulate and examine their membrane proteins." Oh. I see. So nobody has ever thought of this before. No work has ever been done on organisms that are "robust" as a model system. Like - say - thermophiles? Wouldn't that be cool (or hot) to work on.

While most of what I looked at that seemed painful was from outside groups - I wonder whether NSF does any screening of outside press releases before posting them to their News site. Given how bad some of the NSFs press releases are I am not so sure how they deal with outside PR. But why aren't they linking to actual news stories by real journalists? Instead they simply link to PRs from groups supported by NSF. Yuck.

"These kinds of adaptations are likely to allow microorganisms like Halorubrum lacusprofundi to survive not only in Antarctica, but elsewhere in the universe," says Dr. DasSarma.

What? Does he really think there will be microorganisms like this elsewhere in the universe? If there is life elsewhere in the universe is it really going to be like this at all?

And then in a shameless attempt to connect to the work being done on Mars:

"For example, there have been recent reports of seasonal flows down the steep sides of craters on Mars suggesting the presence of underground brine pools. Whether microorganisms actually exist in such environments is not yet known, but expeditions like NASA's Curiosity rover are currently looking for signs of life on Mars."

Does this mean in my next PR I should mention Curiosity too?

Actually the most painful part of me is the next paragraph

"Dr. DasSarma and his colleagues are unraveling the basic building blocks of life," says E. Albert Reece, M.D., Ph.D., M.B.A., Vice President for Medical Affairs at the University of Maryland and John Z. and Akiko K. Bowers Distinguished Professor and Dean of the University of Maryland School of Medicine. "Their research into the fundamentals of microbiology are enhancing our understanding of life throughout the universe, and I look forward to seeing further groundbreaking discoveries from their laboratory."

First - do they really need to list that Reece is MD, PHD, MBA, VP, Dean and Distinguished Prof? Seriously? Uggh. And then the quotes attributed to said person are not impressive. The basic building blocks of life? Dassarma is not really looking at that. And "life throughout the universe"? Really? What life exactly is that? And finally, "further groundbreaking discoveries." Just what exactly makes this groundbreaking?

Single-celled organisms are intimately associated with multicellular organisms across the tree of life, and human beings are no exception. Making up 90% of our cellular composition, these invisible passengers (our microbiome) contribute to our health and well-being in crucial ways, including aiding our digestion, the education of our immune system, and resistance to pathogens. Despite this importance, we still lack a fundamental understanding of where our host-associated microbes actually come from. We know that infants are born practically sterile; early-life events such as birth mode can contribute to the types of microbial species found on an individual, but these events cannot adequately explain the majority of spatiotemporal variation observed over a host’s lifetime. To be able to accurately describe the processes that drive host-associated microbial community dynamics, we must have an informed understanding of the role of dispersal in structuring host-associated microbial communities.

Where do they come from? How do they get there? Do these changes (if any) last?

The Green Lab at the University of Oregon-Eugene attempted to answer some of these questions in our latest publication “Significant changes in the skin microbiome mediated by the sport of Roller Derby”, released today by PeerJ. We decided to use Roller Derby as a model system to investigate the role of contact in dispersing skin microbial communities between hosts. We have known for a long time that pathogens can be transmitted via direct contact; could not our commensal microbial communities be shared in this way?

We swabbed the upper arms (a frequent contact point between players during a bout) of players belonging to 3 geographically distinct derby teams and characterized the skin microbiome of each player using 16s rRNA gene Illumina sequencing. We found that each team’s upper arm microbiome was significantly different from one another before play, and that this difference decreased after bouts were played. Not only did teams’ skin microbiomes become less different from one another after play, but the differences were driven in part “by the presence of unique indicator taxa that are commonly associated with human skin, gut, mouth, and respiratory tract.” There were also environmental bacteria associated with soil and plants found in the skin samples.

Although we weren’t able to show a direct link between contact and transfer of specific microbial taxa, the best explanation of the data seems to be that contact between these players during a one-hour bout effectively resulted in homogenization of their upper arm skin microbiomes.

So much yet to explore! As a 2nd year graduate student in the Green Lab I hope to address some of the questions that the Roller Derby paper has brought to our attention. My dissertation research is gearing up to understand the role of dispersal on our skin microbiome. Are some skin sites more amenable to changes than others? Can we pick up host-associated microbes not just from other individuals, but from objects that other individuals have touched? Can we pick up non-host-associated microbes? If we can pick them up, how long do they stick around? How do they participate in the functions attributed to the skin microbiome?

Hope to keep up the fantastic momentum that has been launched by this latest publication – if you have any thoughts or comments, feel free to contact me at abateman@uoregon.edu, or via Twitter: @microbesrock

And you can check out a stop-motion video I made on the skin microbiome here:

The article discusses a new paper which itself sounds potentially interesting. The paper itself sounds somewhat interesting. But that is besides the point. The parts that made me cringe are the inaccurate or overhyped statements about the novelty of this work. Here are some of the statements I find troubling

"While the ability to pilfer genes from another microorganism has been seen before, scientists have never observed this ability in a eukaryote – an organism with a nucleus."

Wow. Completely ludicrous. There are hundreds if not thousands of papers on lateral gene transfer to organisms with nuclei.

“The results give us new insights into evolution,” said co-author Gerald Schoenknecht of Oklahoma State University’s Department of Botany. “Before this, there was not much indication that eukaryotes acquire genes from bacteria.”

Same complaint as above.

"The age of comparative genome sequencing began only slightly more than a decade ago, and revealed a new mechanism of evolution – horizontal gene transfer – that would not have been discovered any other way,” said co-author Matt Kane, program director in the National Science Foundation’s (NSF) Division of Environmental Biology. “This finding extends our understanding of the role that this mechanism plays in evolution to eukaryotic microorganisms."

I hoped that this was a misquote because the person quoted is Matt Kane - an NSF program officer responsible for many areas related to microbial studies. But alas I found the press release from NSF with the same quote. Perhaps NSF PR people misquoted Matt. I hope they misquoted Matt. Because if not - the quote grossly oversells genome sequencing and what has been learned from it and rather than standing on the shoulders of giants it makes the giants of the past seem like ants.

"It's usually assumed that organisms with a nucleus cannot copy genes from different species--that's why eukaryotes depend on sex to recombine their genomes. "How has Galdieria managed to overcome this limitation? It's an exciting question. What Galdieria did is "a dream come true for biotechnology," says Weber."

This is wrong in so so many ways. Again, as discussed above, eukaryotes have been known to undergo gene transfer for many years.

And to say that the inability to acquire genes by LGT is why eukaryotes depend on sex to recombine their genes? Really? Uggh. As far as I know there are no major theories out there that suggest sex is there because eukaryotes cannot undergo lateral transfer (although certainly some theories on the origin and maintenance of sex do indeed relate to increasing diversity by recombination).

And what makes this a dream come true for Biotech exactly?

I note - this too was in the NSF press release. Has NSF suddenly decided to become like NASA in terms of ludicrous PRs?

I note - I do worry about the effect of calling out NSF on this in terms of my ability to get grants from them. But this is just terrible stuff in this PR and story and it needs to be stopped. I note further that I consider Matt Kane a friend and I hope that he clarifies his quote here and also manages to get NSF to be more rigorous in their PRs.

Saturday, March 02, 2013

In case you have not hear - Nature Publishing Group continues to play around with open publishing and other open science initiatives (when they switch some of their big journals to fully OpenAccess I will stop referring to it as playing around ...). The latest is that Nature has bought into the Frontiers publishing group which publishes a series of Open Access journals. For more on this see: